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南极淡水微藻 , 抑制炎症和癌变。

Antarctic freshwater microalga, , suppresses inflammation and carcinogenesis.

机构信息

Department of Bioscience, Mokpo National University, Muan 58554, Republic of Korea.

Division of Polar Life Sciences, Korea Polar Research Institute, Incheon, 21990, Republic of Korea.

出版信息

Int J Med Sci. 2019 Jan 1;16(2):189-197. doi: 10.7150/ijms.30647. eCollection 2019.

Abstract

Inflammation triggered by the innate immune system is a strategy to protect organisms from the risk of environmental infection. However, it has recently become clear that inflammation can cause a variety of human diseases, including cancer. In this study, we investigated the effects of an ethanol extract of the Antarctic freshwater microalgae, (ETCH), on inflammation and carcinogenesis in RAW 264.7 macrophages and HCT116 human colon cancer cells, respectively. ETCH exhibited significant anti-inflammatory activity through the dose-dependent modulation of major inflammatory markers such as COX-2, IL-6, iNOS, TNF-α, and NO production. For example, ETCH reduced LPS-induced upregulation of COX-2, IL-6, iNOS, and TNF- alpha mRNA levels, leading to a significant decrease in the levels of LPS-stimulated NO and IL-6 as well as TNF-alpha products. In contract, ETCH exhibited dose-dependent cytotoxic activity against HCT116 cells, yielding a profound reduction in the proliferation of the cancer cells. Furthermore, ETCH induced G2 phase cell cycle arrest by transcriptionally regulating of genes involved in G2 / M transition including p21 (CDKN1A), cyclin B1 (CCNB1), and CDK1; CDKN1A mRNA levels were upregulated in response to ETCH, whereas CCNB1 and CDK1 were downregulated. This study reports for the first time anti-inflammatory and anti-cancer effects of, . and provides new insights into the molecular mechanisms of the linkage between inflammation and cancer.

摘要

天然免疫系统引发的炎症是一种保护生物体免受环境感染风险的策略。然而,最近人们清楚地认识到,炎症可以引起多种人类疾病,包括癌症。在这项研究中,我们分别研究了南极淡水微藻的乙醇提取物(ETCH)对 RAW 264.7 巨噬细胞和 HCT116 人结肠癌细胞中炎症和癌变的影响。ETCH 通过对主要炎症标志物(如 COX-2、IL-6、iNOS、TNF-α 和 NO 产生)的剂量依赖性调节,表现出显著的抗炎活性。例如,ETCH 降低了 LPS 诱导的 COX-2、IL-6、iNOS 和 TNF-α mRNA 水平的上调,导致 LPS 刺激的 NO 和 IL-6 以及 TNF-α 产物水平显著降低。相反,ETCH 对 HCT116 细胞表现出剂量依赖性细胞毒性活性,导致癌细胞的增殖显著减少。此外,ETCH 通过转录调节 G2/M 转换相关基因(包括 p21(CDKN1A)、细胞周期蛋白 B1(CCNB1)和 CDK1)诱导 G2 期细胞周期停滞;ETCH 响应上调 CDKN1A mRNA 水平,而 CCNB1 和 CDK1 下调。本研究首次报道了 的抗炎和抗癌作用,为炎症与癌症之间的联系提供了新的分子机制见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58d5/6367532/75aa442ac552/ijmsv16p0189g001.jpg

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